Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-32018
Wydenkeller, S. Electrophysiological Markers for Neuropathic Pain in Spinal Cord Injured Subjects. 2009, University of Zurich / ETH Zurich, Faculty of Medicine.
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Physical disability following spinal cord injury (SCI) is the most striking problem noted
by the general public. But for the affected subjects urogenital difficulties or
depression and pain are often more burdensome. Pain after SCI can have various
reasons but only neuropathic pain below the level of lesion (bNP) is thought to be
caused by injury of the spinal nervous tissue. This type of pain is in the focus of this
thesis. Once bNP has established it is mostly chronic and medication is generally
ineffective. Currently, more and more treatments trying to restore function after SCI
enter the clinical trial phase. Besides improving function, however, treatments
increasing nerve growth in the spinal cord risk to induce or exacerbate bNP.
Therefore, observation of bNP is a crucial factor in such interventional studies. A
method to objectively supervise bNP has, however, not yet been established.
The spinothalamic tract (STT) mainly transmits nociceptive and temperature
information in the spinal cord. This tract was dysfunctional in SCI subjects suffering
from bNP in clinical examinations. Nevertheless, STT dysfunction was not predictive
for bNP and sensory differences between subjects with and without bNP could not be
detected. In contrast to clinical examination which is always subjective and only
offers limited resolution, electrophysiological measures allow for a more detailed and
The novel electrophysiological method of contact heat evoked potentials (CHEP)
measures STT function. Establishment of this method was the goal of the first study.
The painful stimulation on locations along the spine allowed the calculation of the
conduction velocity of the STT in healthy subjects. Furthermore the CHEP latency
depended linearly on the heat pain threshold with 1° C higher threshold leading to
approximately 10 ms longer latency. It was hypothesized that the rather low heating
rate combined with the time-consuming passive heat spread from skin surface to
nociceptors was responsible for this.
The second study aimed at clarifying this dependence through comparison of the
results of study 1 with those of a theoretical heat transfer model. According to this
model, 1° C higher pain threshold leads to approximately 15 ms longer CHEP
latency. The close similarity between the experimentally determined (study 1) and the
computed dependence, proved the influence of the pain threshold on CHEP latency.
Electrophysiological markers for Neuropathic Pain in SCI Subjects 2
Subjects suffering from neuropathic pain (NP) in general and not only in SCI, have
lowered EEG peak frequency. It was hypothesized in literature that the reduced EEG
peak frequency emerged from thalamic deafferentiation and from the ensuing
dysrhythmia in thalamocortical feedback loops. Therefore, the third study
investigated EEG peak frequency in addition to STT function and compared both
between SCI subjects with and without bNP and controls. The STT function
(measured with CHEP) below the level of injury was distinctly impaired in SCI
compared to control subjects. Furthermore, the EEG peak frequency was generally
lower in the SCI subjects. While the CHEP measurements did not reveal differences
between subjects with and without bNP, the EEG peak frequency was lowered in
subjects with bNP. This difference, however, was only apparent after the linear
dependence of EEG peak frequency from the level of SCI was taken into account. In
consideration of this dependence, the EEG peak frequency could in future be helpful
to supervise bNP both in studies aiming at restoring function or reducing pain after
Currently, the clinical read-out parameter for STT function is pinprick sensation. In
the fourth study this pinprick sensation was traced over the first year after SCI.
Comparison of this STT function with the bNP state of the same subjects 2-5 years
after SCI disclosed larger functional STT recovery in subjects suffering from bNP.
Despite the different STT functional recovery, the initial and end measurements did
not discriminate between subjects with and without bNP. This was in agreement with
earlier studies. The results corroborate the above mentioned hypothesis that new
therapies intending to promote sensorimotor recovery after SCI could simultaneously
induce bNP by boosting recovery of spinothalamic function.
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|Referees:||Schwab M E|
|Communities & Collections:||04 Faculty of Medicine > Brain Research Institute|
|DDC:||570 Life sciences; biology
610 Medicine & health
|Deposited On:||23 Feb 2010 08:40|
|Last Modified:||09 Jul 2012 04:16|
|Number of Pages:||82|
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